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therefore be utilized as an internal reference (
54
). Recent data
suggest
31
P MRS is ideal for investigating cortical energy metabo-
lism following SAH, as it allows for quantifi cation of adenosine
triphosphate (ATP).
6. Future
Directions
and Conclusions
Despite intense clinical and scientifi c investigation, the understand-
ing of SAH has advanced slowly since Walter Dandy performed the
fi rst clipping of a cerebral aneurysm in 1931. Considerable atten-
tion has been focused on the elucidation mechanisms underlying
cerebral vasospasm, as this leads to signifi cant death and morbidity
following SAH, with little improvement in clinical outcomes.
Recent literature suggests a second mechanism of acute injury
resulting from global ischemia, referred to as early brain injury.
Additional research must be performed in order to delineate the
critic pathways involved.
Recent advances in technology, such as MRS, CBF monitor-
ing, cortical EEG, and microdialysis, have provided new opportu-
nities for exploration. These minimally invasive modalities can be
utilized to allow a greater understanding of critical physiologic and
biochemical cascades following SAH. Currently, these events are
poorly understood; the development of complications, such as
vasospasm, cannot be predicted or effectively treated. Recent data
have described spreading waves of neuronal and glial depolariza-
tion following SAH, which have been spatially and temporally
linked to delayed ischemic lesions that develop days after an SAH
(
26
). These depolarizations have been demonstrated in healthy
brain and are thought to aid in energy delivery to neurons;
conversely, under pathologic conditions they contribute to energy
failure and worsen injury (Fig.
5
). Understanding the complex
electrophysiologic events during the acute phase of injury is critical
to advancing our treatment strategies and improving patient
outcomes.
References
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2. Moriwaki T, Takagi Y, Sadamasa N, Aoki T,
Nozaki K, Hashimoto N (2006) Impaired pro-
gression of cerebral aneurysms in interleukin-
1beta-defi cient mice. Stroke 37(3):900-905
3. Voldby B, Enevoldsen EM (1982) Intracranial
pressure changes following aneurysm rupture.
Part 1: clinical and angiographic correlations.
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4. Bederson JB, Germano IM, Guarino L (1995)
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Acute vasoconstriction after subarachnoid
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6. Kamiya K, Kuyama H, Symon L (1983) An
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subarachnoid hemorrhage. J Neurosurg 59:
917-924
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